Th2 cytokines inhibit lymphangiogenesis.
Identifieur interne : 000C45 ( PubMed/Checkpoint ); précédent : 000C44; suivant : 000C46Th2 cytokines inhibit lymphangiogenesis.
Auteurs : Ira L. Savetsky [États-Unis] ; Swapna Ghanta [États-Unis] ; Jason C. Gardenier [États-Unis] ; Jeremy S. Torrisi [États-Unis] ; Gabriela D. García Nores [États-Unis] ; Geoffrey E. Hespe [États-Unis] ; Matthew D. Nitti [États-Unis] ; Raghu P. Kataru [États-Unis] ; Babak J. Mehrara [États-Unis]Source :
- PloS one [ 1932-6203 ] ; 2015.
Descripteurs français
- KwdFr :
- Animaux, Cellules endothéliales (cytologie), Cellules endothéliales (immunologie), Interleukine-13 (immunologie), Interleukine-4 (immunologie), Lymphangiogenèse (immunologie), Lymphocytes auxiliaires Th2 (cytologie), Lymphocytes auxiliaires Th2 (immunologie), Mouvement cellulaire (immunologie), Mâle, Prolifération cellulaire, Souris, Survie cellulaire (immunologie).
- MESH :
English descriptors
- KwdEn :
- MESH :
- chemical , immunology : Interleukin-13, Interleukin-4.
- cytology : Endothelial Cells, Th2 Cells.
- immunology : Cell Movement, Cell Survival, Endothelial Cells, Lymphangiogenesis, Th2 Cells.
- Animals, Cell Proliferation, Male, Mice.
Abstract
Lymphangiogenesis is the process by which new lymphatic vessels grow in response to pathologic stimuli such as wound healing, inflammation, and tumor metastasis. It is well-recognized that growth factors and cytokines regulate lymphangiogenesis by promoting or inhibiting lymphatic endothelial cell (LEC) proliferation, migration and differentiation. Our group has shown that the expression of T-helper 2 (Th2) cytokines is markedly increased in lymphedema, and that these cytokines inhibit lymphatic function by increasing fibrosis and promoting changes in the extracellular matrix. However, while the evidence supporting a role for T cells and Th2 cytokines as negative regulators of lymphatic function is clear, the direct effects of Th2 cytokines on isolated LECs remains poorly understood. Using in vitro and in vivo studies, we show that physiologic doses of interleukin-4 (IL-4) and interleukin-13 (IL-13) have profound anti-lymphangiogenic effects and potently impair LEC survival, proliferation, migration, and tubule formation. Inhibition of these cytokines with targeted monoclonal antibodies in the cornea suture model specifically increases inflammatory lymphangiogenesis without concomitant changes in angiogenesis. These findings suggest that manipulation of anti-lymphangiogenic pathways may represent a novel and potent means of improving lymphangiogenesis.
DOI: 10.1371/journal.pone.0126908
PubMed: 26039103
Affiliations:
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pubmed:26039103Le document en format XML
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It is well-recognized that growth factors and cytokines regulate lymphangiogenesis by promoting or inhibiting lymphatic endothelial cell (LEC) proliferation, migration and differentiation. Our group has shown that the expression of T-helper 2 (Th2) cytokines is markedly increased in lymphedema, and that these cytokines inhibit lymphatic function by increasing fibrosis and promoting changes in the extracellular matrix. However, while the evidence supporting a role for T cells and Th2 cytokines as negative regulators of lymphatic function is clear, the direct effects of Th2 cytokines on isolated LECs remains poorly understood. Using in vitro and in vivo studies, we show that physiologic doses of interleukin-4 (IL-4) and interleukin-13 (IL-13) have profound anti-lymphangiogenic effects and potently impair LEC survival, proliferation, migration, and tubule formation. Inhibition of these cytokines with targeted monoclonal antibodies in the cornea suture model specifically increases inflammatory lymphangiogenesis without concomitant changes in angiogenesis. These findings suggest that manipulation of anti-lymphangiogenic pathways may represent a novel and potent means of improving lymphangiogenesis.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26039103</PMID><DateCreated><Year>2015</Year><Month>06</Month><Day>04</Day></DateCreated><DateCompleted><Year>2016</Year><Month>02</Month><Day>22</Day></DateCompleted><DateRevised><Year>2016</Year><Month>10</Month><Day>19</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>10</Volume><Issue>6</Issue><PubDate><Year>2015</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS ONE</ISOAbbreviation></Journal><ArticleTitle>Th2 cytokines inhibit lymphangiogenesis.</ArticleTitle><Pagination><MedlinePgn>e0126908</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0126908</ELocationID><Abstract><AbstractText>Lymphangiogenesis is the process by which new lymphatic vessels grow in response to pathologic stimuli such as wound healing, inflammation, and tumor metastasis. It is well-recognized that growth factors and cytokines regulate lymphangiogenesis by promoting or inhibiting lymphatic endothelial cell (LEC) proliferation, migration and differentiation. Our group has shown that the expression of T-helper 2 (Th2) cytokines is markedly increased in lymphedema, and that these cytokines inhibit lymphatic function by increasing fibrosis and promoting changes in the extracellular matrix. However, while the evidence supporting a role for T cells and Th2 cytokines as negative regulators of lymphatic function is clear, the direct effects of Th2 cytokines on isolated LECs remains poorly understood. Using in vitro and in vivo studies, we show that physiologic doses of interleukin-4 (IL-4) and interleukin-13 (IL-13) have profound anti-lymphangiogenic effects and potently impair LEC survival, proliferation, migration, and tubule formation. Inhibition of these cytokines with targeted monoclonal antibodies in the cornea suture model specifically increases inflammatory lymphangiogenesis without concomitant changes in angiogenesis. These findings suggest that manipulation of anti-lymphangiogenic pathways may represent a novel and potent means of improving lymphangiogenesis.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Savetsky</LastName><ForeName>Ira L</ForeName><Initials>IL</Initials><AffiliationInfo><Affiliation>The Department of Surgery, Division of Plastic and Reconstructive Surgery, Memorial Sloan Kettering Cancer Center, New York, New York, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ghanta</LastName><ForeName>Swapna</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>The Department of Surgery, Division of Plastic and Reconstructive Surgery, Memorial Sloan Kettering Cancer Center, New York, New York, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gardenier</LastName><ForeName>Jason C</ForeName><Initials>JC</Initials><AffiliationInfo><Affiliation>The Department of Surgery, Division of Plastic and Reconstructive Surgery, Memorial Sloan Kettering Cancer Center, New York, New York, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Torrisi</LastName><ForeName>Jeremy S</ForeName><Initials>JS</Initials><AffiliationInfo><Affiliation>The Department of Surgery, Division of Plastic and Reconstructive Surgery, Memorial Sloan Kettering Cancer Center, New York, New York, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>García Nores</LastName><ForeName>Gabriela D</ForeName><Initials>GD</Initials><AffiliationInfo><Affiliation>The Department of Surgery, Division of Plastic and Reconstructive Surgery, Memorial Sloan Kettering Cancer Center, New York, New York, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hespe</LastName><ForeName>Geoffrey E</ForeName><Initials>GE</Initials><AffiliationInfo><Affiliation>The Department of Surgery, Division of Plastic and Reconstructive Surgery, Memorial Sloan Kettering Cancer Center, New York, New York, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nitti</LastName><ForeName>Matthew D</ForeName><Initials>MD</Initials><AffiliationInfo><Affiliation>The Department of Surgery, Division of Plastic and Reconstructive Surgery, Memorial Sloan Kettering Cancer Center, New York, New York, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kataru</LastName><ForeName>Raghu P</ForeName><Initials>RP</Initials><AffiliationInfo><Affiliation>The Department of Surgery, Division of Plastic and Reconstructive Surgery, Memorial Sloan Kettering Cancer Center, New York, New York, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mehrara</LastName><ForeName>Babak J</ForeName><Initials>BJ</Initials><AffiliationInfo><Affiliation>The Department of Surgery, Division of Plastic and Reconstructive Surgery, Memorial Sloan Kettering Cancer Center, New York, New York, United States of America.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>P30 CA008748</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL111130</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 CA009501</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL111130-01</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>06</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018793">Interleukin-13</NameOfSubstance></Chemical><Chemical><RegistryNumber>207137-56-2</RegistryNumber><NameOfSubstance UI="D015847">Interleukin-4</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Am J Pathol. 2010 Dec;177(6):3202-14</RefSource><PMID Version="1">21056998</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Methods. 2003 Jul;30(3):256-68</RefSource><PMID Version="1">12798140</PMID></CommentsCorrections><CommentsCorrections 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Version="1">23193171</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Commun. 2015;6:6196</RefSource><PMID Version="1">25648335</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002465" MajorTopicYN="N">Cell Movement</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002470" MajorTopicYN="N">Cell Survival</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D042783" MajorTopicYN="N">Endothelial Cells</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018793" MajorTopicYN="N">Interleukin-13</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015847" MajorTopicYN="N">Interleukin-4</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D042583" MajorTopicYN="N">Lymphangiogenesis</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018418" MajorTopicYN="N">Th2 Cells</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC4454507</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>02</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>03</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>6</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>6</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>2</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26039103</ArticleId><ArticleId IdType="doi">10.1371/journal.pone.0126908</ArticleId><ArticleId IdType="pii">PONE-D-15-07585</ArticleId><ArticleId IdType="pmc">PMC4454507</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>État de New York</li></region></list><tree><country name="États-Unis"><region name="État de New York"><name sortKey="Savetsky, Ira L" sort="Savetsky, Ira L" uniqKey="Savetsky I" first="Ira L" last="Savetsky">Ira L. Savetsky</name></region><name sortKey="Garcia Nores, Gabriela D" sort="Garcia Nores, Gabriela D" uniqKey="Garcia Nores G" first="Gabriela D" last="García Nores">Gabriela D. García Nores</name><name sortKey="Gardenier, Jason C" sort="Gardenier, Jason C" uniqKey="Gardenier J" first="Jason C" last="Gardenier">Jason C. Gardenier</name><name sortKey="Ghanta, Swapna" sort="Ghanta, Swapna" uniqKey="Ghanta S" first="Swapna" last="Ghanta">Swapna Ghanta</name><name sortKey="Hespe, Geoffrey E" sort="Hespe, Geoffrey E" uniqKey="Hespe G" first="Geoffrey E" last="Hespe">Geoffrey E. Hespe</name><name sortKey="Kataru, Raghu P" sort="Kataru, Raghu P" uniqKey="Kataru R" first="Raghu P" last="Kataru">Raghu P. Kataru</name><name sortKey="Mehrara, Babak J" sort="Mehrara, Babak J" uniqKey="Mehrara B" first="Babak J" last="Mehrara">Babak J. Mehrara</name><name sortKey="Nitti, Matthew D" sort="Nitti, Matthew D" uniqKey="Nitti M" first="Matthew D" last="Nitti">Matthew D. Nitti</name><name sortKey="Torrisi, Jeremy S" sort="Torrisi, Jeremy S" uniqKey="Torrisi J" first="Jeremy S" last="Torrisi">Jeremy S. Torrisi</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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